Dataset Information

Unrestricted Feed Intake Induces ?-Cell Death and Impairs Insulin Secretion in Broiler Breeder Hens.

ABSTRACT: Past studies regarding to insulin secretion and glucose disposal in chickens were focused on rapidly growing juvenile broilers and may not reflect glucose/insulin physiology in adulthood. The study aimed to assess insulin secretion and glucose disposal in respect to restricted (R) vs. ad libitum (Ad) feed intake for obesity development in broiler breeder hens. Hens at age of 26 weeks were continued on R rations, or allowed Ad-feed intake up to 45 weeks. Results from prandial changes and glucose tolerance test suggested that Ad-feed intake to 45 weeks impaired insulin secretion and glucose clearance, and, thus, caused hyperglycemia in accompany with transient hyperinsulinemia at age of 33 weeks (p < 0.05). The alterations were shown operating at both transcript and protein level of insulin gene expression per se and at ATP supply for insulin release as evidenced by consistent changes of enzyme expression and activity in pyruvate anaplerosis in the ?-islets (p < 0.05). Ad-feed intake also increased ?-islet triacylglycerol and ceramide accumulation and provoked interleukin-1? (IL-1?) production (p < 0.05), which were further manifested by a detrimental increase of caspase 3/7 activity and cell apoptosis (p < 0.05). Results support the conclusion that release to Ad-feed intake in broiler breeder hens transiently induced hyperinsulinemia along rapid bodyweight gain and adiposity, but later provoked lipotoxicity and inflammation leading to ?-cell apoptosis and ultimately impaired insulin secretion and glucose disposal.

SUBMITTER: Huang YF

PROVIDER: S-EPMC7693285 | biostudies-literature | 2020 Oct

REPOSITORIES: biostudies-literature

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Unrestricted Feed Intake Induces β-Cell Death and Impairs Insulin Secretion in Broiler Breeder Hens.

Huang Yu-Feng YF Chang Ling-Chu LC Chen Chung-Yu CY Chen Yu-Hui YH Walzem Rosemary L RL Chen Shuen-Ei SE

Animals : an open access journal from MDPI 20201026 11

Past studies regarding to insulin secretion and glucose disposal in chickens were focused on rapidly growing juvenile broilers and may not reflect glucose/insulin physiology in adulthood. The study aimed to assess insulin secretion and glucose disposal in respect to restricted (R) vs. ad libitum (Ad) feed intake for obesity development in broiler breeder hens. Hens at age of 26 weeks were continued on R rations, or allowed Ad-feed intake up to 45 weeks. Results from prandial changes and glucose ...[more]

PMID: 33114772

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Project description:Ad libitumfeeding in broiler breeder (BB) hens causes reduced egg production, lower fertility, and improper eggshell deposition. Restricted feeding (RF) is the only effective intervention available to normalize ovarian function and improve reproductive efficiency. This study aimed to assess the transcriptional changes in ovarian cortex of BB hens with free access to feed compared to those on a RF diet. RNA was isolated from the ovarian cortex of Cobb 500 pullets raised to 10 and 16 weeks of age on either a full-feeding (FF) or RF diet. Microarray analysis identified 386 differentially expressed genes between the two feeding groups at 16 weeks of age. Gene ontology enrichment identified overrepresentation of Neuroactive ligand-receptor interaction pathways, Cell adhesion molecules, Steroid hormone biosynthesis, and various KEGG pathways. From these groups, 46 genes were selected for follow-up validation by quantitative PCR. The findings show that 33 of the 46 genes had significantly different abundance by age and/or feeding level. Most of these genes were repressed in RF hens and belonged to the steroid biosynthesis and neuropeptide signaling groups. The VIPR2 receptor was higher in the FF group leading us to hypothesize that vasoactive intestinal peptide (VIP) is an important regulator of small cortical follicles. Culture of hen cortical follicles with VIP increased Star, an indication of increased steroidogenic activity, although did not elevate Cyp11a1. These results offer insights and suggest the possible mechanisms and pathways responsible for the increases in cortical follicle growth associated with excess feed intake in BB hens.Lay summaryGiving breeder hens unrestricted access to feed can lead to problems with their ovaries, including excessive growth of the ovary and reduced fertility. Giving a limited amount of feed is the only effective way to reduce this growth of the ovaries and improve fertility. This study aimed to assess the changes in the molecules that make proteins in the body in hens fed unrestricted and restricted diets. In the hens fed a limited amount of feed, there were more of one type of molecules, while there were more of another type in the ovaries of hens with unrestricted access to feed. These results show that how much a hen eats can alter the number of these molecules in the ovary and this could help us understand why their ovaries grow excessively and why their eggs are less fertile.

Project description:The effect of ME intake (MEI) on the reproductive system was evaluated. Ross 308 broiler breeder pullets (n = 140) were assigned to 2 treatments from 22 to 26 wk of age: (1) Low-energy diet fed restricted (2,807 kcal/kg, low MEI) and (2) high-energy diet fed unrestricted (3,109 kcal/kg, high MEI). Daylength was increased from 8 to 14 h at 22 wk of age with a light intensity of 30 lux. Daily palpation was used to detect sexual maturity via the presence of a hard-shelled egg in the shell gland. Expression of gonadotropin releasing hormone-I (GnRH) and gonadotropin inhibitory hormone (GnIH) genes in the hypothalamus and GnRH receptor (GnRH-RI) and GnIH receptor (GnIH-R) genes in the anterior pituitary gland of each pullet was evaluated from 22 to 26 wk of age using quantitative real time-PCR. Blood samples were taken weekly and luteinizing hormone (LH), follicle stimulating-hormone (FSH), and 17-beta-estradiol (E2) determined using commercial ELISA kits. Carcass samples were used for determination of CP and fat content. Data were analyzed using the MIXED procedure in SAS, and differences were reported where P ≤ 0.05. High MEI treatment pullets had 2.3-fold higher GnRH and 1.8-fold higher GnRH-RI mRNA levels than low MEI pullets. MEI affected neither expression of GnIH and GnIH-R nor carcass protein content. For high MEI (489 kcal/D) and low MEI treatments (258 kcal/D), respectively, from 22 to 26 wk of age (P ≤ 0.05), LH concentration was 3.05 and 1.60 ng/mL; FSH concentration was 145 and 89.3 pg/mL; E2 concentration was 429 and 266 pg/mL, and carcass lipid was 13.9 and 10.3%. The onset of lay for pullets in the high MEI treatment advanced such that 100% had laid by 26 wk of age compared with 30% in the low MEI treatment. We concluded that higher MEI advanced the activation of the hypothalamic-pituitary-gonadal axis and also increased body lipid deposition, and moreover, stimulated reproductive hormone levels which overall accelerated puberty in broiler breeder pullets.

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Project description:A supplement of 69 ?g 25-hydroxycholecalciferol (25-OH-D3)/kg feed increased livability in feed restricted (R-hens) broiler breeder hens by 9.9% and by 65.6% in hens allowed ad libitum feed intake (Ad-hens) in a feeding trial from age 26-60 weeks. Hens with higher bodyweight and/or adiposity suffered sudden death (SD) earlier in conjunction with compromised heart rhythms and over-ventilation. In the study with the same flock of hens, we demonstrate that 25-OH-D3 improved hen's livability and heart health by ameliorating systemic hypoxia, acidosis, and cardiac pathological hypertrophy through calcineurin-NFAT4c signaling and MHC- expression in association with reduced plasma triacylglycerol and hepatic steatosis and fibrosis (p < 0.05). In contrast to live hens sampled at 29, 35, and 47 weeks, SD hens exhibited severe cardiac hypertrophy that was either progressive (Ad-groups) or stable (R-groups). Actual and relative liver weights in SD hens from any group declined as the study progressed. Heart weight correlated significantly to total and relative liver weights in SD-hens of both R- and Ad-groups. In contrast to normal counterparts sampled at 35 and 47 weeks, R-hens exhibiting cardiac hypertrophy experienced severe hypoxia and acidosis, with increased bodyweight, absolute and relative weights of liver and heart, hepatic and plasma triacylglycerol content, and cardiac arrhythmia (p < 0.05). The present results demonstrate that pathological cardiac hypertrophy and functional failure are causative factors of SD and this pathogenic progression is accelerated by hepatopathology, particularly during the early age. Increased feed efficiency with rapid gains in BW and fat increase hens' risk for hypoxia, irreversible cardiac hypertrophy, and arrhythmias that cause functional compromise and SD. Additional supplementation of 69 mg/kg feed of 25-OH-D3 to the basal diet is effective to ameliorate cardiac pathogenesis and prevent SD in broiler breeder hens.

Dataset Information

Unrestricted Feed Intake Induces ?-Cell Death and Impairs Insulin Secretion in Broiler Breeder Hens.

Publications

Unrestricted Feed Intake Induces β-Cell Death and Impairs Insulin Secretion in Broiler Breeder Hens.

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